Intrahypothalamic secretion of angiotensin II in response to immunological or non-immunological stress in rats : a microdialysis study

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We previously reported that brain angiotensin II (ANG II) receptors contribute to the fever induced by immunological or non-immunological stress in rats. The present study was carried out to investigate whether immunological [prostaglandin E_2 (PGE_2) injection] or non-immunological (immobilization) stress elicits the secretion of ANG II in the hypothalamus in rats, using microdialysis technique. Our microdialysis study (perfusion flow rate=2 μl/min and recovery rate=14.2%) showed that, during intrahypothalamic perfusion with PGE_2 (2 μg/2 μl perfusate/min), ANG II release in the hypothalamus could be detected by the presence of a small amount of ANG II in the perfusate (on average, 0.17 pg/2 μl perfusate/min ; n=3). Such a release of ANG II did not occur during vehicle infusion (n=4). It is therefore reasonable to consider that PGE_2 in the hypothalamus binds to intrahypothalamic PGE receptors, which results in ANG II release. Subsequently, ANG II released within the hypothalamus might modulate the PGE_2-induced febrile responses. In contrast, when rats were exposed to immobilization stress, no secretion of ANG II was detected in the rat's hypothalamus. Since the recovery rate of the microdialysis probe used in this study was 14.2% and the peptide is so unstable, actual secretion of ANG II might have been unable to be measured. Technical improvement is necessary to detect such a small amount of the peptide, for example by using the inhibitors of the enzyme which inactivates the peptide.